The Experts below are selected from a list of 144 Experts worldwide ranked by ideXlab platform
John L Robertson - One of the best experts on this subject based on the ideXlab platform.
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dimethylarsinic acid in drinking water changed the morphology of urinary bladder but not the expression of dna repair genes of bladder Transitional Epithelium in f344 rats
Toxicologic Pathology, 2009Co-Authors: Amy Wang, Douglas C Wolf, Geremy W Knapp, Steven D Holladay, William R Huckle, Thomas Caceci, John L RobertsonAbstract:Inorganic arsenic increasesurinary bladderTransitionalcellcarcinoma inhumans. InF344rats, dimethylarsinicacid(DMA[V])increases Transitional cell carcinoma. Arsenic-induced inhibition of DNA repair has been reported in cultured cell lines and in lymphocytes of arsenic-exposed humans, but it has not been studied in urinary bladder. Should inhibition of DNA damage repair in Transitional Epithelium occur, it may contribute to carcinogenesi so r cocarcinogenesis. We investigated morphology and expression of DNA repair genes in F344 rat Transitional cells following up to 100 ppm DMA(V) in drinking water for four weeks. Mitochondria were very sensitive to DMA(V), and swollen mitochondria appeared to be the main source of vacuoles in the Transitional Epithelium. Real-time reverse transcriptase polymerase chain reaction (Real-Time RT PCR) showed the mRNA levels of tested DNA repair genes, ataxia telangectasia mutant (ATM), X-ray repair cross-complementing group 1 (XRCC1), excision repair cross-complementing group 3/xeroderma pigmentosum B (ERCC3/XPB), and DNA polymerase b (Polb), were not altered by DMA(V). These data suggested that either DMA(V) does not affect DNA repair in the bladder or DMA(V) affects DNA repair without affecting baseline mRNA levels of repair genes. The possibilityremains thatDMA(V) may lower damage-inducedincreases inrepairgeneexpressionor cause post-translational modificationofrepairenzymes.
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Dimethylarsinic acid in drinking water changed the morphology of urinary bladder but not the expression of DNA repair genes of bladder Transitional Epithelium in F344 rats.
Toxicologic pathology, 2009Co-Authors: Amy Wang, Douglas C Wolf, Geremy W Knapp, Steven D Holladay, William R Huckle, Thomas Caceci, Banalata Sen, John L RobertsonAbstract:Inorganic arsenic increasesurinary bladderTransitionalcellcarcinoma inhumans. InF344rats, dimethylarsinicacid(DMA[V])increases Transitional cell carcinoma. Arsenic-induced inhibition of DNA repair has been reported in cultured cell lines and in lymphocytes of arsenic-exposed humans, but it has not been studied in urinary bladder. Should inhibition of DNA damage repair in Transitional Epithelium occur, it may contribute to carcinogenesi so r cocarcinogenesis. We investigated morphology and expression of DNA repair genes in F344 rat Transitional cells following up to 100 ppm DMA(V) in drinking water for four weeks. Mitochondria were very sensitive to DMA(V), and swollen mitochondria appeared to be the main source of vacuoles in the Transitional Epithelium. Real-time reverse transcriptase polymerase chain reaction (Real-Time RT PCR) showed the mRNA levels of tested DNA repair genes, ataxia telangectasia mutant (ATM), X-ray repair cross-complementing group 1 (XRCC1), excision repair cross-complementing group 3/xeroderma pigmentosum B (ERCC3/XPB), and DNA polymerase b (Polb), were not altered by DMA(V). These data suggested that either DMA(V) does not affect DNA repair in the bladder or DMA(V) affects DNA repair without affecting baseline mRNA levels of repair genes. The possibilityremains thatDMA(V) may lower damage-inducedincreases inrepairgeneexpressionor cause post-translational modificationofrepairenzymes.
Amy Wang - One of the best experts on this subject based on the ideXlab platform.
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dimethylarsinic acid in drinking water changed the morphology of urinary bladder but not the expression of dna repair genes of bladder Transitional Epithelium in f344 rats
Toxicologic Pathology, 2009Co-Authors: Amy Wang, Douglas C Wolf, Geremy W Knapp, Steven D Holladay, William R Huckle, Thomas Caceci, John L RobertsonAbstract:Inorganic arsenic increasesurinary bladderTransitionalcellcarcinoma inhumans. InF344rats, dimethylarsinicacid(DMA[V])increases Transitional cell carcinoma. Arsenic-induced inhibition of DNA repair has been reported in cultured cell lines and in lymphocytes of arsenic-exposed humans, but it has not been studied in urinary bladder. Should inhibition of DNA damage repair in Transitional Epithelium occur, it may contribute to carcinogenesi so r cocarcinogenesis. We investigated morphology and expression of DNA repair genes in F344 rat Transitional cells following up to 100 ppm DMA(V) in drinking water for four weeks. Mitochondria were very sensitive to DMA(V), and swollen mitochondria appeared to be the main source of vacuoles in the Transitional Epithelium. Real-time reverse transcriptase polymerase chain reaction (Real-Time RT PCR) showed the mRNA levels of tested DNA repair genes, ataxia telangectasia mutant (ATM), X-ray repair cross-complementing group 1 (XRCC1), excision repair cross-complementing group 3/xeroderma pigmentosum B (ERCC3/XPB), and DNA polymerase b (Polb), were not altered by DMA(V). These data suggested that either DMA(V) does not affect DNA repair in the bladder or DMA(V) affects DNA repair without affecting baseline mRNA levels of repair genes. The possibilityremains thatDMA(V) may lower damage-inducedincreases inrepairgeneexpressionor cause post-translational modificationofrepairenzymes.
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Dimethylarsinic acid in drinking water changed the morphology of urinary bladder but not the expression of DNA repair genes of bladder Transitional Epithelium in F344 rats.
Toxicologic pathology, 2009Co-Authors: Amy Wang, Douglas C Wolf, Geremy W Knapp, Steven D Holladay, William R Huckle, Thomas Caceci, Banalata Sen, John L RobertsonAbstract:Inorganic arsenic increasesurinary bladderTransitionalcellcarcinoma inhumans. InF344rats, dimethylarsinicacid(DMA[V])increases Transitional cell carcinoma. Arsenic-induced inhibition of DNA repair has been reported in cultured cell lines and in lymphocytes of arsenic-exposed humans, but it has not been studied in urinary bladder. Should inhibition of DNA damage repair in Transitional Epithelium occur, it may contribute to carcinogenesi so r cocarcinogenesis. We investigated morphology and expression of DNA repair genes in F344 rat Transitional cells following up to 100 ppm DMA(V) in drinking water for four weeks. Mitochondria were very sensitive to DMA(V), and swollen mitochondria appeared to be the main source of vacuoles in the Transitional Epithelium. Real-time reverse transcriptase polymerase chain reaction (Real-Time RT PCR) showed the mRNA levels of tested DNA repair genes, ataxia telangectasia mutant (ATM), X-ray repair cross-complementing group 1 (XRCC1), excision repair cross-complementing group 3/xeroderma pigmentosum B (ERCC3/XPB), and DNA polymerase b (Polb), were not altered by DMA(V). These data suggested that either DMA(V) does not affect DNA repair in the bladder or DMA(V) affects DNA repair without affecting baseline mRNA levels of repair genes. The possibilityremains thatDMA(V) may lower damage-inducedincreases inrepairgeneexpressionor cause post-translational modificationofrepairenzymes.
Thomas Caceci - One of the best experts on this subject based on the ideXlab platform.
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dimethylarsinic acid in drinking water changed the morphology of urinary bladder but not the expression of dna repair genes of bladder Transitional Epithelium in f344 rats
Toxicologic Pathology, 2009Co-Authors: Amy Wang, Douglas C Wolf, Geremy W Knapp, Steven D Holladay, William R Huckle, Thomas Caceci, John L RobertsonAbstract:Inorganic arsenic increasesurinary bladderTransitionalcellcarcinoma inhumans. InF344rats, dimethylarsinicacid(DMA[V])increases Transitional cell carcinoma. Arsenic-induced inhibition of DNA repair has been reported in cultured cell lines and in lymphocytes of arsenic-exposed humans, but it has not been studied in urinary bladder. Should inhibition of DNA damage repair in Transitional Epithelium occur, it may contribute to carcinogenesi so r cocarcinogenesis. We investigated morphology and expression of DNA repair genes in F344 rat Transitional cells following up to 100 ppm DMA(V) in drinking water for four weeks. Mitochondria were very sensitive to DMA(V), and swollen mitochondria appeared to be the main source of vacuoles in the Transitional Epithelium. Real-time reverse transcriptase polymerase chain reaction (Real-Time RT PCR) showed the mRNA levels of tested DNA repair genes, ataxia telangectasia mutant (ATM), X-ray repair cross-complementing group 1 (XRCC1), excision repair cross-complementing group 3/xeroderma pigmentosum B (ERCC3/XPB), and DNA polymerase b (Polb), were not altered by DMA(V). These data suggested that either DMA(V) does not affect DNA repair in the bladder or DMA(V) affects DNA repair without affecting baseline mRNA levels of repair genes. The possibilityremains thatDMA(V) may lower damage-inducedincreases inrepairgeneexpressionor cause post-translational modificationofrepairenzymes.
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Dimethylarsinic acid in drinking water changed the morphology of urinary bladder but not the expression of DNA repair genes of bladder Transitional Epithelium in F344 rats.
Toxicologic pathology, 2009Co-Authors: Amy Wang, Douglas C Wolf, Geremy W Knapp, Steven D Holladay, William R Huckle, Thomas Caceci, Banalata Sen, John L RobertsonAbstract:Inorganic arsenic increasesurinary bladderTransitionalcellcarcinoma inhumans. InF344rats, dimethylarsinicacid(DMA[V])increases Transitional cell carcinoma. Arsenic-induced inhibition of DNA repair has been reported in cultured cell lines and in lymphocytes of arsenic-exposed humans, but it has not been studied in urinary bladder. Should inhibition of DNA damage repair in Transitional Epithelium occur, it may contribute to carcinogenesi so r cocarcinogenesis. We investigated morphology and expression of DNA repair genes in F344 rat Transitional cells following up to 100 ppm DMA(V) in drinking water for four weeks. Mitochondria were very sensitive to DMA(V), and swollen mitochondria appeared to be the main source of vacuoles in the Transitional Epithelium. Real-time reverse transcriptase polymerase chain reaction (Real-Time RT PCR) showed the mRNA levels of tested DNA repair genes, ataxia telangectasia mutant (ATM), X-ray repair cross-complementing group 1 (XRCC1), excision repair cross-complementing group 3/xeroderma pigmentosum B (ERCC3/XPB), and DNA polymerase b (Polb), were not altered by DMA(V). These data suggested that either DMA(V) does not affect DNA repair in the bladder or DMA(V) affects DNA repair without affecting baseline mRNA levels of repair genes. The possibilityremains thatDMA(V) may lower damage-inducedincreases inrepairgeneexpressionor cause post-translational modificationofrepairenzymes.
William R Huckle - One of the best experts on this subject based on the ideXlab platform.
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dimethylarsinic acid in drinking water changed the morphology of urinary bladder but not the expression of dna repair genes of bladder Transitional Epithelium in f344 rats
Toxicologic Pathology, 2009Co-Authors: Amy Wang, Douglas C Wolf, Geremy W Knapp, Steven D Holladay, William R Huckle, Thomas Caceci, John L RobertsonAbstract:Inorganic arsenic increasesurinary bladderTransitionalcellcarcinoma inhumans. InF344rats, dimethylarsinicacid(DMA[V])increases Transitional cell carcinoma. Arsenic-induced inhibition of DNA repair has been reported in cultured cell lines and in lymphocytes of arsenic-exposed humans, but it has not been studied in urinary bladder. Should inhibition of DNA damage repair in Transitional Epithelium occur, it may contribute to carcinogenesi so r cocarcinogenesis. We investigated morphology and expression of DNA repair genes in F344 rat Transitional cells following up to 100 ppm DMA(V) in drinking water for four weeks. Mitochondria were very sensitive to DMA(V), and swollen mitochondria appeared to be the main source of vacuoles in the Transitional Epithelium. Real-time reverse transcriptase polymerase chain reaction (Real-Time RT PCR) showed the mRNA levels of tested DNA repair genes, ataxia telangectasia mutant (ATM), X-ray repair cross-complementing group 1 (XRCC1), excision repair cross-complementing group 3/xeroderma pigmentosum B (ERCC3/XPB), and DNA polymerase b (Polb), were not altered by DMA(V). These data suggested that either DMA(V) does not affect DNA repair in the bladder or DMA(V) affects DNA repair without affecting baseline mRNA levels of repair genes. The possibilityremains thatDMA(V) may lower damage-inducedincreases inrepairgeneexpressionor cause post-translational modificationofrepairenzymes.
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Dimethylarsinic acid in drinking water changed the morphology of urinary bladder but not the expression of DNA repair genes of bladder Transitional Epithelium in F344 rats.
Toxicologic pathology, 2009Co-Authors: Amy Wang, Douglas C Wolf, Geremy W Knapp, Steven D Holladay, William R Huckle, Thomas Caceci, Banalata Sen, John L RobertsonAbstract:Inorganic arsenic increasesurinary bladderTransitionalcellcarcinoma inhumans. InF344rats, dimethylarsinicacid(DMA[V])increases Transitional cell carcinoma. Arsenic-induced inhibition of DNA repair has been reported in cultured cell lines and in lymphocytes of arsenic-exposed humans, but it has not been studied in urinary bladder. Should inhibition of DNA damage repair in Transitional Epithelium occur, it may contribute to carcinogenesi so r cocarcinogenesis. We investigated morphology and expression of DNA repair genes in F344 rat Transitional cells following up to 100 ppm DMA(V) in drinking water for four weeks. Mitochondria were very sensitive to DMA(V), and swollen mitochondria appeared to be the main source of vacuoles in the Transitional Epithelium. Real-time reverse transcriptase polymerase chain reaction (Real-Time RT PCR) showed the mRNA levels of tested DNA repair genes, ataxia telangectasia mutant (ATM), X-ray repair cross-complementing group 1 (XRCC1), excision repair cross-complementing group 3/xeroderma pigmentosum B (ERCC3/XPB), and DNA polymerase b (Polb), were not altered by DMA(V). These data suggested that either DMA(V) does not affect DNA repair in the bladder or DMA(V) affects DNA repair without affecting baseline mRNA levels of repair genes. The possibilityremains thatDMA(V) may lower damage-inducedincreases inrepairgeneexpressionor cause post-translational modificationofrepairenzymes.
Geremy W Knapp - One of the best experts on this subject based on the ideXlab platform.
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dimethylarsinic acid in drinking water changed the morphology of urinary bladder but not the expression of dna repair genes of bladder Transitional Epithelium in f344 rats
Toxicologic Pathology, 2009Co-Authors: Amy Wang, Douglas C Wolf, Geremy W Knapp, Steven D Holladay, William R Huckle, Thomas Caceci, John L RobertsonAbstract:Inorganic arsenic increasesurinary bladderTransitionalcellcarcinoma inhumans. InF344rats, dimethylarsinicacid(DMA[V])increases Transitional cell carcinoma. Arsenic-induced inhibition of DNA repair has been reported in cultured cell lines and in lymphocytes of arsenic-exposed humans, but it has not been studied in urinary bladder. Should inhibition of DNA damage repair in Transitional Epithelium occur, it may contribute to carcinogenesi so r cocarcinogenesis. We investigated morphology and expression of DNA repair genes in F344 rat Transitional cells following up to 100 ppm DMA(V) in drinking water for four weeks. Mitochondria were very sensitive to DMA(V), and swollen mitochondria appeared to be the main source of vacuoles in the Transitional Epithelium. Real-time reverse transcriptase polymerase chain reaction (Real-Time RT PCR) showed the mRNA levels of tested DNA repair genes, ataxia telangectasia mutant (ATM), X-ray repair cross-complementing group 1 (XRCC1), excision repair cross-complementing group 3/xeroderma pigmentosum B (ERCC3/XPB), and DNA polymerase b (Polb), were not altered by DMA(V). These data suggested that either DMA(V) does not affect DNA repair in the bladder or DMA(V) affects DNA repair without affecting baseline mRNA levels of repair genes. The possibilityremains thatDMA(V) may lower damage-inducedincreases inrepairgeneexpressionor cause post-translational modificationofrepairenzymes.
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Dimethylarsinic acid in drinking water changed the morphology of urinary bladder but not the expression of DNA repair genes of bladder Transitional Epithelium in F344 rats.
Toxicologic pathology, 2009Co-Authors: Amy Wang, Douglas C Wolf, Geremy W Knapp, Steven D Holladay, William R Huckle, Thomas Caceci, Banalata Sen, John L RobertsonAbstract:Inorganic arsenic increasesurinary bladderTransitionalcellcarcinoma inhumans. InF344rats, dimethylarsinicacid(DMA[V])increases Transitional cell carcinoma. Arsenic-induced inhibition of DNA repair has been reported in cultured cell lines and in lymphocytes of arsenic-exposed humans, but it has not been studied in urinary bladder. Should inhibition of DNA damage repair in Transitional Epithelium occur, it may contribute to carcinogenesi so r cocarcinogenesis. We investigated morphology and expression of DNA repair genes in F344 rat Transitional cells following up to 100 ppm DMA(V) in drinking water for four weeks. Mitochondria were very sensitive to DMA(V), and swollen mitochondria appeared to be the main source of vacuoles in the Transitional Epithelium. Real-time reverse transcriptase polymerase chain reaction (Real-Time RT PCR) showed the mRNA levels of tested DNA repair genes, ataxia telangectasia mutant (ATM), X-ray repair cross-complementing group 1 (XRCC1), excision repair cross-complementing group 3/xeroderma pigmentosum B (ERCC3/XPB), and DNA polymerase b (Polb), were not altered by DMA(V). These data suggested that either DMA(V) does not affect DNA repair in the bladder or DMA(V) affects DNA repair without affecting baseline mRNA levels of repair genes. The possibilityremains thatDMA(V) may lower damage-inducedincreases inrepairgeneexpressionor cause post-translational modificationofrepairenzymes.
